Murray P.J., Allen J.E., Biswas S.K., Fisher E.A., Gilroy D.W., Goerdt S., Gordon S., Hamilton J.A., Ivashkiv L.B., Lawrence T. i wsp.: Macrophage activation and polarization: Nomenclature and experimental guidelines. Immunity, 2014; 41: 14-20
Xue J., Schmidt S.V., Sander J., Draffehn A., Krebs W., Quester I., De Nardo D., Gohel T.D., Emde M., Schmidleithner L. i wsp.: Transcriptome-based network analysis reveals a spectrum model of human macrophage activation. Immunity, 2014; 40: 274-288
Ginhoux F., Greter M., Leboeuf M., Nandi S., See P., Gokhan S., Mehler M.F., Conway S.J., Ng L.G., Stanley E.R. i wsp.: Fate mapping analysis reveals that adult microglia derive from primitive macrophages. Science, 2010; 330: 841-845
Cherry J.D., Olschowka J.A., O’Banion M.K.: Neuroinflammation and M2 microglia: The good, the bad, and the inflamed. J. Neuro-inflammation, 2014; 11: 98
Raciborski F., Gawińska E., Kłak A., Słowik A., Wnuk M.: Udary mózgu: rosnący problem w starzejącym się społeczeństwie. Instytut Ochrony Zdrowia w Polsce, Warszawa 2016
Morrison H.W., Filosa J.A.: A quantitative spatiotemporal analysis of microglia morphology during ischemic stroke and reperfusion. J. Neuroinflammation, 2013; 10: 4
Perego C., Fumagalli S., De Simoni M.G.: Temporal pattern of expression and colocalization of microglia/macrophage phenotype markers following brain ischemic injury in mice. J. Neuroinflammation, 2011; 8: 174
Li T., Pang S., Yu Y., Wu X., Guo J., Zhang S.: Proliferation of parenchymal microglia is the main source of microgliosis after ischaemic stroke. Brain, 2013; 136: 3578-3588
Schilling M., Besselmann M., Müller M., Strecker J.K., Ringel-stein E.B., Kiefer R.: Predominant phagocytic activity of resident microglia over hematogenous macrophages following transient focal cerebral ischemia: An investigation using green fluorescent protein transgenic bone marrow chimeric mice. Exp. Neurol., 2005; 196: 290-297
Emerich D.F., Dean R.L.3rd, Bartus R.T.: The role of leukocytes following cerebral ischemia: Pathogenic variable or bystander reaction to emerging infarct? Exp. Neurol., 2002; 173: 168-181
Nilupul Perera M., Ma H.K., Arakawa S., Howells D.W., Markus R., Rowe C.C., Donnan G.A.: Inflammation following stroke. J. Clin. Neurosci., 2006; 13: 1-8
Xiong X.Y., Liu L., Yang Q.W.: Functions and mechanisms of microglia/macrophages in neuroinflammation and neurogenesis after stroke. Prog. Neurobiol., 2016; 142: 23-44
Gelderblom M., Weymar A., Bernreuther C., Velden J., Arunachalam P., Steinbach K., Orthey E., Arumugam T.V., Leypoldt F., Simova O. i wsp.: Neutralization of the IL-17 axis diminishes neutrophil invasion and protects from ischemic stroke. Blood, 2012; 120: 3793-3802
Gelosa P., Lecca D., Fumagalli M., Wypych D., Pignieri A., Cimino M., Verderio C., Enerbäck M., Nikookhesal E., Tremoli E. i wsp.: Microglia is a key player in the reduction of stroke damage promoted by the new antithrombotic agent ticagrelor. J. Cereb. Blood Flow Metab., 2014; 34: 979-988
Riboldi E., Porta C., Morlacchi S., Viola A., Mantovani A., Sica A.: Hypoxia-mediated regulation of macrophage functions in patho-physiology. Int. Immunol., 2013; 25: 67-75
Girard S., Brough D., Lopez-Castejon G., Giles J., Rothwell N.J., Allan S.M.: Microglia and macrophages differentially modulate cell death after brain injury caused by oxygen-glucose deprivation in organotypic brain slices. Glia, 2013; 61: 813-824
Yamasaki R., Lu H., Butovsky O., Ohno N., Rietsch A.M., Cialic R., Wu P.M., Doykan C.E., Lin J., Cotleur A.C. i wsp.: Differential roles of microglia and monocytes in the inflamed central nervous system. J. Exp. Med., 2014; 211: 1533-1549
Wattananit S., Tornero D., Graubardt N., Memanishvili T., Monni E., Tatarishvili J., Miskinyte G., Ge R., Ahlenius H., Lindvall O. i wsp.: Monocyte-derived macrophages contribute to spontaneous long-term functional recovery after stroke in mice. J. Neurosci., 2016; 36: 4182-4195
Zhao X., Sun G., Zhang J., Strong R., Song W., Gonzales N., Grotta J.C., Aronowski J.: Hematoma resolution as a target for intracerebral hemorrhage treatment: Role for peroxisome proliferator-activated receptor γ in microglia/macrophages. Ann. Neurol., 2007; 61: 352-362
Lin S., Yin Q., Zhong Q., Lv F.L., Zhou Y., Li J.Q., Wang J.Z., Su B.Y., Yang Q.W.: Heme activates TLR4-mediated inflammatory injury via MyD88/TRIF signaling pathway in intracerebral hemorrhage. J. Neuroinflammation, 2012; 9: 46
Fang H., Chen J., Lin S., Wang P., Wang Y., Xiong X., Yang Q.: CD36-mediated hematoma absorption following intracerebral hemorrhage: Negative regulation by TLR4 signaling. J. Immunol, 2014; 192: 5984-5992
Suenaga J., Hu X., Pu H., Shi Y., Hassan S.H., Xu M., Leak R.K., Stetler R.A., Gao Y., Chen J.: White matter injury and microglia/ macrophage polarization are strongly linked with age-related longterm deficits in neurological function after stroke. Exp. Neurol., 2015; 272: 109-119
Taylor R.A., Hammond M.D., Ai Y., Sansing L.H.: CX3CR1-null microglia fail to transition to an M2 phenotype after intracerebral hemorrhage. Stroke, 2015; 46: A114-A114
Nikodemova M., Duncan I.D., Watters J.J.: Minocycline exerts inhibitory effects on multiple mitogen-activated protein kinases and IκBα degradation in a stimulus-specific manner in microglia. J. Neurochem., 2006; 96: 314-323
Malhotra K., Chang J.J., Khunger A., Blacker D., Switzer J.A., Goyal N., Hernandez A.V., Pasupuleti V., Alexandrov A.V., Tsivgoulis G.: Minocycline for acute stroke treatment: A systematic review and meta-analysis of randomized clinical trials. J. Neurol., 2018; 265: 1871-1879
Pan J., Jin J.L., Ge H.M., Yin K.L., Chen X., Han L.J., Chen Y., Qian L., Li X.X., Xu Y.: Malibatol A regulates microglia M1/M2 polarization in experimental stroke in a PPARγ-dependent manner. J. Neuroinflammation, 2015; 12: 51
Han L., Cai W., Mao L., Liu J., Li P., Leak R.K., Xu Y., Hu X., Chen J.: Rosiglitazone promotes white matter integrity and long-term functional recovery after focal cerebral ischemia. Stroke, 2015; 46: 2628-2636
Desestret V., Riou A., Chauveau F., Cho T.H., Devillard E., Marinescu M., Ferrera R., Rey C., Chanal M., Angoulvant D. i wsp.: In vitro and in vivo models of cerebral ischemia show discrepancy in therapeutic effects of M2 macrophages. PLoS One, 2013; 8: e67063
Kigerl K.A., Gensel J.C., Ankeny D.P., Alexander J.K., Donnelly D.J., Popovich P.G.: Identification of two distinct macrophage subsets with divergent effects causing either neurotoxicity or regeneration in the injured mouse spinal cord. J. Neurosci., 2009; 29: 13435-13444
Wang X., Cao K., Sun X., Chen Y., Duan Z., Sun L., Guo L., Bai P., Sun D., Fan J. i wsp.: Macrophages in spinal cord injury: Phenotypic and functional change from exposure to myelin debris. Glia, 2015; 63: 635-651
Galtrey C.M., Fawcett J.W.: The role of chondroitin sulfate proteoglycans in regeneration and plasticity in the central nervous system. Brain Res. Rev., 2007; 54: 1-18
Zhang Y., Liu Z., Zhang W., Wu Q., Zhang Y., Liu Y., Guan Y., Chen X.: Melatonin improves functional recovery in female rats after acute spinal cord injury by modulating polarization of spinal microglial/macrophages. J. Neurosci. Res., 2019; 97: 733-743
Wegiel J., Wang K.C., Imaki H., Rubenstein R., Wronska A., Osuchowski M., Lipinski W.J., Walker L.C., LeVine H.: The role of microglial cells and astrocytes in fibrillar plaque evolution in transgenic APP(SW) mice. Neurobiol. Aging, 2001; 22: 49-61
Colton C.A., Mott R.T., Sharpe H., Xu Q., van Nostrand W.E., Vitek M.P.: Expression profiles for macrophage alternative activation genes in AD and in mouse models of AD. J. Neuroinflammation, 2006; 3: 27
Simard A.R., Soulet D., Gowing G., Julien J.P., Rivest S.: Bone marrow-derived microglia play a critical role in restricting senile plaque formation in Alzheimer’s disease. Neuron, 2006; 49: 489502
Hoozemans J.J., Veerhuis R., Rozemuller J.M., Eikelenboom P.: Neuroinflammation and regeneration in the early stages of Alzheimer’s disease pathology. Int. J. Dev. Neurosci., 2006; 24: 157-165
Bhaskar K., Konerth M., Kokiko-Cochran O.N., Cardona A., Ransohoff R.M., Lamb B.T.: Regulation of tau pathology by the microglial fractalkine receptor. Neuron, 2010; 68: 19-31
Koenigsknecht-Talboo J., Landreth G.E.: Microglial phagocytosis induced by fibrillar β-amyloid and IgGs are differentially regulated by proinflammatory cytokines. J. Neurosci., 2005; 25: 8240-8249
Yamamoto M., Kiyota T., Walsh S.M., Liu J., Kipnis J., Ikezu T.: Cytokine-mediated inhibition of fibrillar amyloid-β peptide degradation by human mononuclear phagocytes. J. Immunol., 2008; 181: 3877-3886
Su X.Q., Wang X.Y., Gong F.T., Feng M., Bai J.J., Zhang R.R., Dang X.Q.: Oral treatment with glycyrrhizin inhibits NLRP3 inflammasome activation and promotes microglial M2 polarization after traumatic spinal cord injury. Brain Res. Bull., 2020; 158: 1-8
Yamanaka M., Ishikawa T., Griep A., Axt D., Kummer M.P., Heneka M.T.: PPARγ/RXRα-induced and CD36-mediated microglial amyloid-β phagocytosis results in cognitive improvement in amyloid precursor protein/presenilin 1 mice. J. Neurosci., 2012; 32: 17321-17331
Oh S., Son M., Choi J., Lee S., Byun K.: sRAGE prolonged stem cell survival and suppressed RAGE-related inflammatory cell and T lymphocyte accumulations in an Alzheimer’s disease model. Biochem. Biophys. Res. Commun., 2018; 495: 807-813
Ratti E., Berry J.D.: Amyotrophic lateral sclerosis 1 and many diseases. W: Genomics, Circuits, and Pathways in Clinical Neuropsychiatry, red.: T. Lehner, B.L. Miller, M.W. State. Academic Press, San Diego 2016, 685-712
Boillée S., Yamanaka K., Lobsiger C.S., Copeland N.G., Jenkins N.A., Kassiotis G., Kollias G., Cleveland D.W.: Onset and progression in inherited ALS determined by motor neurons and microglia. Science, 2006; 312: 1389-1392
Xiao Q., Zhao W., Beers D.R., Yen A.A., Xie W., Henkel J.S., Appel S.H.: Mutant SOD1G93A microglia are more neurotoxic relative to wild-type microglia. J. Neurochem., 2007; 102: 2008-2019
Geloso M.C., Corvino V., Marchese E., Serrano A., Michetti F., D’Ambrosi N.: The dual role of microglia in ALS: Mechanisms and therapeutic approaches. Front. Aging Neurosci., 2017; 9: 242
Liao B., Zhao W., Beers D.R., Henkel J.S., Appel S.H.: Transformation from a neuroprotective to a neurotoxic microglial phenotype in a mouse model of ALS. Exp. Neurol., 2012; 237: 147-152
Gravel M., Béland L.C., Soucy G., Abdelhamid E., Rahimian R., Gravel C., Kriz J.: IL-10 controls early microglial phenotypes and disease onset in ALS caused by misfolded superoxide dismutase1. J. Neurosci., 2016; 36: 1031-1048
Chiu I.M., Chen A., Zheng Y., Kosaras B., Tsiftsoglou S.A., Vartanian T.K., Brown R.H.Jr., Carroll M.C.: T lymphocytes potentiate endogenous neuroprotective inflammation in a mouse model of ALS. Proc. Natl. Acad. Sci. USA, 2008; 105: 17913-17918
Lewis K.E., Rasmussen A.L., Bennett W., King A., West A.K., Chung R.S., Chuah M.I.: Microglia and motor neurons during disease progression in the SOD1G93A mouse model of amyotrophic lateral sclerosis: Changes in arginase1 and inducible nitric oxide synthase. J. Neuroinflammation, 2014; 11: 55
Shin T., Ahn M., Matsumoto Y.: Mechanism of experimental autoimmune encephalomyelitis in Lewis rats: Recent insights from macrophages. Anat. Cell Biol., 2012; 45: 141-148
Bauer J., Sminia T., Wouterlood F.G., Dijkstra C.D.: Phagocytic activity of macrophages and microglial cells during the course of acute and chronic relapsing experimental autoimmune encephalomyelitis. J. Neurosci. Res., 1994; 38: 365-375
Ponomarev E.D., Shriver L.P., Maresz K., Dittel B.N.: Microglial cell activation and proliferation precedes the onset of CNS autoimmunity. J. Neurosci. Res., 2005; 81: 374-389
Ransohoff R.M., Engelhardt B.: The anatomical and cellular basis of immune surveillance in the central nervous system. Nat. Rev. Immunol., 2012; 12: 623-635
Renno T., Krakowski M., Piccirillo C., Lin J.Y., Owens T.: TNF-alpha expression by resident microglia and infiltrating leukocytes in the central nervous system of mice with experimental allergic encephalomyelitis. Regulation by Th1 cytokines. J. Immunol., 1995; 154: 944-953
Zhao W., Tilton R.G., Corbett J.A., McDaniel M.L., Misko T.P., Williamson J.R., Cross A.H., Hickey W.F.: Experimental allergic encephalomyelitis in the rat is inhibited by aminoguanidine, an inhibitor of nitric oxide synthase. J. Neuroimmunol., 1996; 64: 123-133
Chu F., Shi M., Zheng C., Shen D., Zhu J., Zheng X., Cui L.: The roles of macrophages and microglia in multiple sclerosis and experimental autoimmune encephalomyelitis. J. Neuroimmunol., 2018; 318: 1-7
Ahn M., Yang W., Kim H., Jin J.K., Moon C., Shin T.: Immunohistochemical study of arginase-1 in the spinal cords of Lewis rats with experimental autoimmune encephalomyelitis. Brain Res., 2012; 1453: 77-86
Ponomarev E.D., Maresz K., Tan Y., Dittel B.N.: CNS-derived interleukin-4 is essential for the regulation of autoimmune inflammation and induces a state of alternative activation in microglial cells. J. Neurosci., 2007; 27: 10714-10721
Mikita J., Dubourdieu-Cassagno N., Deloire M.S., Vekris A., Biran M., Raffard G., Brochet B., Canron M.H., Franconi J.M., Boiziau C., Petry K.G.: Altered M1/M2 activation patterns of monocytes in severe relapsing experimental rat model of multiple sclerosis. Amelioration of clinical status by M2 activated monocyte administration. Mult. Scler. J., 2011; 17: 2-15
Moreno M., Bannerman P., Ma J., Guo F., Miers L., Soulika A.M., Pleasure D.: Conditional ablation of astroglial CCL2 suppresses CNS accumulation of M1 macrophages and preserves axons in mice with MOG peptide EAE. J. Neurosci., 2014; 34: 8175-8185
Benedek G., Zhang J., Nguyen H., Kent G., Seifert H., Vandenbark A.A., Offner H.: Novel feedback loop between M2 macrophages/microglia and regulatory B cells in estrogen-protected EAE mice. J. Neuroimmunol., 2017; 305: 59-67
Tierney J.B., Kharkrang M., La Flamme A.C.: Type II-activated macrophages suppress the development of experimental autoimmune encephalomyelitis. Immunol. Cell Biol., 2009; 87: 235-240
Ponomarev E.D., Veremeyko T., Weiner H.L.: MicroRNAs are universal regulators of differentiation, activation, and polarization of microglia and macrophages in normal and diseased CNS. Glia, 2013; 61: 91-103
Yang Y., Ye Y., Kong C., Su X., Zhang X., Bai W., He X.: MiR-124 enriched exosomes promoted the M2 polarization of microglia and enhanced hippocampus neurogenesis after traumatic brain injury by inhibiting TLR4 pathway. Neurochem. Res., 2019; 44: 811-828
Imler T.J.Jr., Petro T.M.: Decreased severity of experimental autoimmune encephalomyelitis during resveratrol administration is associated with increased IL-17+IL-10+ T cells, CD4- IFN-γ+ cells, and decreased macrophage IL-6 expression. Int. Immunopharmacol., 2009; 9: 134-143
Lühder F., Lee D.H., Gold R., Stegbauer J., Linker R.A.: Small but powerful: Short peptide hormones and their role in autoimmune inflammation. J. Neuroimmunol., 2009; 217: 1-7
Yang Q., Zheng C., Cao J., Cao G., Shou P., Lin L., Velletri T., Jiang M., Chen Q., Han Y. i wsp.: Spermidine alleviates experimental autoimmune encephalomyelitis through inducing inhibitory macrophages. Cell Death Differ., 2016; 23: 1850-1861
Liu C.Y., Guo S.D., Yu J.Z., Li Y.H., Zhang H., Feng L., Chai Z., Yuan H.J., Yang W.F., Feng Q.J. i wsp.: Fasudil mediates cell therapy of EAE by immunomodulating encephalomyelitic T cells and macrophages. Eur. J. Immunol., 2015; 45: 142-152
Bhasin M., Wu M., Tsirka S.E.: Modulation of microglial/macrophage activation by macrophage inhibitory factor (TKP) or tuftsin (TKPR) attenuates the disease course of experimental autoimmune encephalomyelitis. BMC Immunol., 2007; 8: 10
Nissen J.C., Selwood D.L., Tsirka S.E.: Tuftsin signals through its receptor neuropilin-1 via the transforming growth factor beta pathway. J. Neurochem., 2013; 127: 394-402